ReviewDiabetes, obesity & metabolism2026
Therapies for Cardiovascular-Kidney-Liver-Metabolic Syndrome: Reappraisal of Fibrates.
Review in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Therapies for Cardiovascular-Kidney-Liver-Metabolic Syndrome: Reappraisal of Fibrates.Diabetes, obesity & metabolism · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Cardiovascular disease, chronic kidney disease (CKD), type 2 diabetes mellitus (T2DM), obesity and metabolic dysfunction-associated steatohepatitis (MASH) frequently coexist and share overlapping pathophysiology, forming the proposed cardiovascular-kidney-liver-metabolic (CKLM) syndrome. Although contemporary therapies such as sodium-glucose cotransporter-2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and non-steroidal mineralocorticoid receptor antagonists (nsMRA) have improved cardiovascular and renal outcomes, diabetes-related microvascular complications remain common. Fibrates, traditionally used to lower triglycerides and increase high-density lipoprotein cholesterol, activate peroxisome proliferator-activated receptor-α (PPAR-α) and influence pathways involved in metabolic and vascular injury, including inflammation, oxidative stress, endothelial dysfunction, mitochondrial metabolism, lipid handling, fibrosis and angiogenesis. This review reappraises the potential role of fibrates within the CKLM syndrome framework, focusing on diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, peripheral artery disease and metabolic dysfunction-associated steatotic liver disease. Clinical evidence is the strongest for diabetic retinopathy, where fenofibrate reduces retinopathy progression and the need for retinal laser therapy. Post hoc analyses also suggest favourable effects on albuminuria progression and chronic estimated glomerular filtration rate (eGFR) decline, although fibrates may cause a reversible rise in serum creatinine. Evidence for diabetic neuropathy remains limited, while clinical trials and real-world studies suggest reductions in lower-extremity amputations and diabetic foot complications. In liver disease, fenofibrate has shown modest benefit, whereas selective PPAR-α modulators may more favourably influence liver enzymes, inflammation and non-invasive fibrosis markers. Overall, fibrates may complement contemporary cardiometabolic therapies by targeting residual microvascular and liver-related risk. However, dedicated outcome trials and improved patient stratification are needed before broader clinical implementation.
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